Although it is commonly understood that we are what we eat, this is clearly not the case for dietary fats. To remain weight stable, most of us are luckily able to burn almost all of what we eat each year, including the few hundred thousand kilocalories of fat that we ingest. This constant utilization of fats as fuel (fat is the primary energy substrate for liver and resting muscle) allows there to be selectively in the partitioning of specific fats between oxidation and storage in adipose tissue. Evidence for this is seen when we examine human adipose tissue fatty acid composition, as there is a remarkable similarity among samples for people with widely varying dietary practices. In studies of the influence of dietary composition on adipose fatty acids, even the essential fatty acids have correlation coefficients of 0.5 or less, implying that dietary intake determines less than 25% of the variance in adipose fatty acid makeup. Irrefutable evidence for adipocyte selectivity over diet is also found in the regional variation in adipose fatty acid composition within one individual. We have shown a positive gradient in 18:2w6 and its anabolic products in adipose biopsies from the abdomen to the thigh (1.Phinney, AJCN l994), indicating that regional adipose depots have the capability of retaining different proportions of w6 fatty acids (which come only from the diet).

Typically in western industrial nations, human adipose tissue contains more than 50% monounsaturated fatty acids, 30-40% saturates, and 10-20% polyunsaturates. Among the polyunsaturates in adipose triglyceride, one finds predominantly 18:2w6; whereas 18:3w3 is usually < 1%. this paucity of stored 18:3w3 relative to intake is curious, because our typical dietary fats now contain > 1% 18:3w3. There are at least two potential reasons for this disparity between diet and adipose composition. The first is that if 18:3w3 and its anabolic products are truly essential, then a marginal or frankly deficient intake (as proposed by RT Holman, w3 and w6 News, Vol. 1) may result in selective utilization via essential pathways, leaving little excess of storage. The second reason is that there is evidence for selective "non-essential utilization" of 18:3w3 for beta-oxidation both in vitro (2.Raclot and Groscolas, J Lipid Res, l993), and in vivo in rodents (3.Raclot and Grocolas, AJP, l995) and humans (4.Phinney, Lipids, l990; 5.Tang, Lipids, l993).

In these animal and human studies, dietary conditions that reduce body fat stores uniformly resulted in a greater proportionate loss of 18:3w3 from adipose triglyceride than most other long chain fatty acids. Raclot and Groscolas have elegantly demonstrated that the proportional release of specific fatty acids from the adipocyte by hormone sensitive lipase is negatively correlated with chain length and number of double bonds, but positively correlated with the proximity of a double bond to the methyl end of the fatty acid. Thus 18:3w3 is more rapidly mobilized than its positional isomer 18:3w6. That this ultimately leads to net oxidation is underscored by our observation that humans undergoing major weight loss experience a proportionate reduction in adipose triglyceride 18:3w3 reserves (4.Phinney, Lipids, l990), and that this cannot be suppressed by dietary supplementation with 18:3w3 during the weight loss diet (5.Tang, Lipids, l993).

Selective Oxidation cont....

Michael A. Crawford, PhD., FIBiol., FRCPath.,

Institute of Brain Chemistry and Human Nutrition,
University of North London,
166-222 Holloway Road, London N7 8DB, UK.
e-mail: michael@macrawf.co.demon.uk

After finishing my doctorate in chemical pathology at the Royal Post-Graduate Medical School, London in 1960, I worked five years at Makerere Medical School in Uganda. There, I became mainly interested in the pathogenesis of the health problems of Ugandans. Possibly, their propensity to eating huge quantities of green bananas might have had something to do with their intestinal disorders which resulted in volvulus and double volvulus being the #1 reason for surgery: The green banana is rich in serotonin which stimulates intestinal motility. The other unique problem was endomyocardial fibrosis (EMF), a fibrotic condition which affects the endo- and myo-cardium, leading to heart failure and death. But the idea that diet was a factor in EMF did turn out to be right. My experiences in Africa had taught me that nutrition was important.

A subsequent research fellowship with Professor Ernst Baranay at the University of Uppsala, Sweden taught me that the #1 killer in the Western World was coronary heart disease, unheard of in Africans in Uganda. The Swedes suggested it had something to do with the food. I heard in Uppsala a brilliant lecture by Dr. Bang from Denmark on blood cholesterol, arteries and saturated fat. So that narrowed the responsible food down to dietary lipids as a cause of atherosclerosis.

The Different Diseases of Africa and London: no CHD in Africans

Whilst interested in EMF and other fascinating differences in the diseases of Africa and Europe, I felt that it would be a good idea to show my new bosses in London that I was also interested in what Londoners died from. The National Institutes of Health and the Albany Medical Center in Albany, New York in particular, had a major research program running in Uganda, comparing blood cholesterols in Ugandans with Americans (1). The bottom line was that Americans had loads of cholesterol circulating in their blood whereas the Ugandans had half the amount. We had added our little bit by showing that Ugandan, European and North American infants were no different at birth. However, the Europeans could be separated based on a rising blood cholesterol level at six years of age. At that age, the African children's blood cholesterols were little different from those in their first year of life, whereas the European children's levels were substantially higher. African blood pressure also remained singularly stable from childhood to the mid 20s.

Finding the Road to the Home of Poly

It was a cold wintry night back home in London in 1967. We had just installed a machine called an S6 Research Gas Liquid Chromatograph (GLC), and my love affair with POLY was about to begin. She had a black funnel on her roof, a row of red, yellow, green and blue lights above lots of knobs for controlling gas flows, oven temperature, detector, signal amplification, time of day, and a large but efficient pen recorder. She looked like a mock up of Dr. Who's Time Warp Drive for the Tardis! Inside, there was a coil of metal or glass tubing. The idea was that the operator straightened out the metal coil, dangled it in the stair well whilst he tapped in a sandy substance which had previously been laced with polyethylene glycol adipate, Apiezon or something that would grab the methyl esters of fatty acids. The column was re-coiled, replaced, the flow of inert gas adroitly turned on, the temperature raised and methyl esters injected, all of which brought fatty acid esters out the other end, neatly separated in a nice marching order, like soldiers sorted by rank. The glass columns were more difficult. They had to be filled in the coiled state and people regularly broke them. The operator then spent a lot of time injecting onto the column standard mixtures of the methyl esters of palmitic, stearic, linoleic and linolenic acids, and reading everything and anything Bob Ackman had written on the subject (2).

Why Saturated fats are dangerous.....

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